In line with this, enforced expression of p65 in normal thyroid cells caused a moderate but significant increase of miR-182 (Fig. 4d), leading to reversed effects on the expression of Dtx1, HES1, and Notch1 than seen in NThy.RETM918T or TT MTC cell lines in response to miRZIP-182 treatment (Fig. 3e) with a downregulation of HES1 and Notch1 and increased Dtx1 transcript levels (Fig. 4e). Here, HES1 is linked to medullary thyroid gland carcinoma.